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miR‑205‑5p/PTK7 axis is involved in the proliferation, migration and invasion of colorectal cancer cells.

Authors :
ChEN, Shuo
Wang, Yan
Su, Yinan
Zhang, Lin
Zhang, Mingqing
Li, Xueqing
Wang, Juan
Zhang, XipENg
Source :
Molecular Medicine Reports. May2018, Vol. 17 Issue 5, p6253-6260. 8p. 4 Graphs.
Publication Year :
2018

Abstract

MicroRNAs (miRNAs) are small non‑coding RNAs, which are critical in a diverse range of biological processes, including development, differentiation, homeostasis, and in the formation of diseases by accelerating and/or inhibiting the translation of mRNAs. The present study aimed to examine the potential role of miRNA (miR)‑205‑5p in the developmental process of colorectal cancer (CRC) through protein‑tyrosine kinase 7 (PTK7). Initially, TargetScan was used to predict the miRNA target sites in the sequence of the PTK7 3'‑untranslated region. It was then found that the mRNA expression level of miR‑205‑5p was lower in CRC cells, determined using reverse transcription‑quantitative polymerase chain reaction analysis, and there was a negative correlation between miR‑205‑5p and PTK7 in CRC tissues. It was also found that miR‑205‑5p regulated the gene transcription of PTK7, determined using a luciferase reporter assay. The results of RT‑qPCR and western blot analyses in human colorectal cancer revealed that miR‑205‑5p suppressed the expression of PTK7. Finally, it was revealed that miR‑205‑5p restricted the proliferation ability of CRC cells through inhibiting PTK7, which was determined using colony forming and 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assays. miR‑205‑5p accelerated cell apoptosis through inhibiting PTK7, demonstrated using Annexin V‑FITC/propidium iodide staining. The results of a Transwell assay indicated that miR‑205‑5p inhibited the migration and invasion abilities of CRC cells through inhibiting PTK7. Therefore, miR‑205‑5p is involved in the proliferation, migration and invasion of CRC through inhibiting PTK7. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
17912997
Volume :
17
Issue :
5
Database :
Academic Search Index
Journal :
Molecular Medicine Reports
Publication Type :
Academic Journal
Accession number :
129221013
Full Text :
https://doi.org/10.3892/mmr.2018.8650